Abnormal Reactions of Free Radicals and Oxidative Damages in the Bodies of Patients With Chronic Glomerulonephritis

Objective To study the abnormal reactions of a series of free radicals and the oxidative damages induced by free radical abnormal reactions in the bodies of patients with chronic glomerulonephritis. Methods Eighty chronic glomerulonephritis patients (CGNP) and eighty healthy adult volunteers (HAV) were enrolled in a random control study, in which concentrations of nitric oxide (NO) in plasma, lipoperoxides (LPO) in plasma and in erythrocytes, and vitamin C (VC), vitamin E (VE) and beta-carotene (?CAR) in plasma as well as activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) in erythrocytes were determined with spectrophotometric assays. Results Compared with the average values of the above biochemical parameters in the HAV group, the average values of NO in plasma, and LPO in plasma and erythrocytes in the CGNP group were significantly increased (P = 0.0001), while those of VC, VE and -CAR in plasma as well as those of SOD, CAT and GPX in erythrocytes in the CGNP group were significantly decreased (P = 0.0001). Pearson product-moment correlation analysis showed that with increase of the concentration of blood creatinine as well as prolongation of the course of disease in the CGNP, the concentrations of NO in plasma, and LPO in plasma and erythrocytes in the CGNP increased gradually, while the concentrations of VC, VE and ?CAR in plasma as well as the activities of SOD, CAT and GPX in erythrocytes in the CGNP decreased gradually (P = 0.002454 0.000001). The relative risk ratio (RR) of the above biochemical parameters reflecting oxidative damages in the bodies of CGNP ranged from 6.061 to 72.429. The reliability coefficient (alpha) that the above biochemical parameters were used to reflect the oxidative damages of the CGNP was 0.8137, standardized item alpha = 0.9728, Hotelling抯 T-Squared = 1135680.191, F = 53274.6478, P = 0.000001. Conclusions The findings in this study show that in the bodies of CGNP a series of free radical chain reactions result in severe pathological aggravation and induce oxidative damages in their bodies. Therefore, suitable dose of antioxidants should be supplemented to them so as to alleviate oxidative damages in their bodies.

Striatal oxidative damages and neuroinflammation correlate with progression and survival of Lewy body and Alzheimer diseases

Neurodegenerative diseases are a class of chronic and complex disorders featuring progressive loss of neurons in distinct brain areas.The mechanisms responsible for the disease progression in neurodegeneration are not fully illustrated.In this observational study,we have examined diverse biochemical parameters in the caudate and putamen of patients with Lewy body diseases(LBDs)and Alzheimer disease(AD),shedding some light on the involvement of oxidative damage and neuroinflammation in advanced neurodegeneration.We performed Spearman and Mantel-Cox analyses to investigate how oxidative stress and neuroinflammation exert comprehensive effects on disease progression and survival.Disease progression in LBDs correlated positively with poly(ADP-Ribose)and triggering receptors expressed on myeloid cell 2 levels in the striatum of LBD cohorts,indicating that potential parthanatos was a dominant feature of worsening disease progression and might contribute to switching microglial inflammatory phenotypes.Disease progression in AD corresponds negatively with 8-oxo-7,8-dihydro-2′-deoxyguanosine(8-oxo-d G)and myeloperoxidase concentrations in the striatum,suggesting that possible mitochondria dysfunction may be involved in the progression of AD via a mechanism ofβ-amyloid entering the mitochondria and subsequent free radicals generation.Patients with lower striatal 8-oxo-d G and myeloperoxidase levels had a survival advantage in AD.The age of onset also affected disease progression.Tissue requests for the postmortem biochemistry,genetics,and autoradiography studies were approved by the Washington University Alzheimer's Disease Research Center(ADRC)Biospecimens Committee(ethics approval reference number:T1705,approval date:August 6,2019).Recombinant DNA and Hazardous Research Materials were approved by the Washington University Environmental Health&Safety Biological Safety Committee(approval code:3739,approval date:February 25,2020).Radioactive Material Authorization was approved by the Washington University Environmental Health&Safety Radiation Safety Committee(approval code:1056,approval date:September 18,2019).

Reduction of the oxidative damage to H_(2)O_(2)-induced HepG2 cells via the Nrf2 signalling pathway by plant flavonoids Quercetin and Hyperoside

Hyperoside and quercetin are similar in molecular structures.In this study,the antioxidant regulatory targets of hyperoside and quercetin are mainly in the nuclear factor(erythroid-2-derived)-related factor 2(Nrf2)pathway predicted by network pharmacology.And the antioxidant effect and mechanism of hyperoside and quercetin were measured and compared in H_(2)O_(2)-induced Hep G2 cells and Caenorhabditis elegans.The findings indicated that quercetin was more effective than hyperoside in reducing oxidative damage,which was proved by improved cell viability,decreased reactive oxygen species(ROS)production,decreased cellular apoptosis,and alleviated mitochondrial damage.In addition,quercetin was more efficient than hyperoside in enhancing the expression of Nrf2-associated m RNAs,increasing the activities of superoxide dismutase(SOD),glutathione peroxidase(GSH-Px),and catalase(CAT),and reducing the cellular malondialdehyde(MDA)content.Quercetin was superior to hyperoside in prolonging the lifespan of worms,decreasing the accumulation of lipofuscin,inhibiting ROS production,and increasing the proportion of skn-1 in the nucleus.With the Nrf2 inhibitor ML385,we verified that quercetin and hyperoside primarily protected the cells against oxidative damage via the Nrf2 signalling pathway.Furthermore,molecular docking and dynamics simulations demonstrated that the quercetin-Kelch-like ECH-associated protein 1(Keap1)complex was more stable than the hyperoside-Keap1 complex.The stable structure of the complex might hinder the binding of Nrf2 and Keap1 to release Nrf2 and facilitate its entry into the nucleus to play an antioxidant role.Overall,quercetin had a better antioxidant than hyperoside.

Effects of Imazethapyr-Based Herbicide Formulation in the Zebrafish (Danio rerio) Hepatocyte Cell Line (ZF-L): Cytotoxicity and Oxidative Stress

Seizures of agrochemical formulations have increased in Brazil and Rio Grande do Sul is among the Brazilian states with the highest number of seizures of these products obtained illicitly. The use of illicit formulations can cause significant harm to agricultural production, the environment, and non-target species. This study evaluated the cytotoxicity and oxidative stress of a seized formulation containing the herbicide imazethapyr (IMZT). Characterization of the herbicide included gas chromatography-mass spectrometry (GC-MS) and thermal analyses (thermogravimetric analysis (TGA) and differential scanning calorimetry (DSC)). Hemolytic and cytotoxicity assays in ZF-L hepatic cells showed IC50 values of 12.75 µg/mL, 3.01 µg/mL, 2.67 µg/mL, and 1.61 µg/mL for erythrocytes, [3(4,5-dimethyl)-2 bromide-5 diphenyl tetrazolium] (MTT), neutral red (NR), and lactate dehydrogenase (LDH) assays, respectively. The median IC50 of 2.84 µg/mL was used in oxidative stress assays, revealing increased reactive oxygen species (ROS) production, reduced total sulfhydryl content, and decreased superoxide dismutase (SOD) and catalase (CAT) activity. This study is the first to report in vitro oxidative stress induced by IMZT in the ZF-L cell line, emphasizing the importance of in vitro assays for assessing the toxic effects of seized agrochemicals on human health and the environment.

Roles of Aqueous Extract of Marigold on Arsenic-Induced Oxidative Damage in Pancreatic Islet β-Cells

Roles of Marigold extracts (ME) on arsenic trioxide (ATO)-induced oxidative damage to pancreatic β-cells need to be further elucidated. In this study, NIT-1 cells were treated with different concentrations of and/or ATO, following by the cell viability was detected by CCK8 assay. Then, intracellular reactive oxygen species (ROS) levels, lipid peroxide (MDA) contents and superoxide dismutase (SOD) activity were measured with a fluorescence probe method and colorimetric assay, respectively. The apoptosis rate and morphology was detected and observed with hoechst 33,258 staining assay. The mRNA levels and protein expressions of nuclear factor E2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) were measured by real-time fluorescence quantitative polymerase chain reaction and protein immunoblotting assay, respectively. Our results indicated that Co-treatment with ME and ATO exacerbated the cell viability decreasing reduced by ATO, while the addition of ME after ATO treatment effectively promote the recovery of ATO reduced survival rates. The ATO group increased apoptosis (P P β-cells by modulating the activation of the Nrf2 signaling pathway.

The action mechanism by which C1q/tumor necrosis factor-related protein-6 alleviates cerebral ischemia/reperfusion injury in diabetic mice

Studies have shown that C1q/tumor necrosis factor-related protein-6 (CTRP6) can alleviate renal ischemia/reperfusion injury in mice. However, its role in the brain remains poorly understood. To investigate the role of CTRP6 in cerebral ischemia/reperfusion injury associated with diabetes mellitus, a diabetes mellitus mouse model of cerebral ischemia/reperfusion injury was established by occlusion of the middle cerebral artery. To overexpress CTRP6 in the brain, an adeno-associated virus carrying CTRP6 was injected into the lateral ventricle. The result was that oxygen injury and inflammation in brain tissue were clearly attenuated, and the number of neurons was greatly reduced. In vitro experiments showed that CTRP6 knockout exacerbated oxidative damage, inflammatory reaction, and apoptosis in cerebral cortical neurons in high glucose hypoxia-simulated diabetic cerebral ischemia/reperfusion injury. CTRP6 overexpression enhanced the sirtuin-1 signaling pathway in diabetic brains after ischemia/reperfusion injury. To investigate the mechanism underlying these effects, we examined mice with depletion of brain tissue-specific sirtuin-1. CTRP6-like protection was achieved by activating the sirtuin-1 signaling pathway. Taken together, these results indicate that CTRP6 likely attenuates cerebral ischemia/reperfusion injury through activation of the sirtuin-1 signaling pathway.

Consilience and unity in ocular anterior segment research

In his beautiful book,Consilience:The Unity of Knowledge,the eminent biologist Edward O Wilson,advocates the need for integration and reconciliation across the sciences.He defines consilience as“literally a‘jumping together’of knowledge with a linking of facts…to create a common groundwork of explanation”.It is the premise of this paper that as much as basic biomedical research is in need of data generation using the latest available techniques–unifying available knowledge is just as critical.This involves the necessity to resolve contradictory findings,reduce silos,and acknowledge complexity.We take the cornea and the lens as case studies of our premise.Specifically,in this perspective,we discuss the conflicting and fragmented information on protein aggregation,oxidative damage,and fibrosis.These are fields of study that are integrally tied to anterior segment research.Our goal is to highlight the vital need for Wilson’s consilience and unity of knowledge which in turn should lead to enhanced rigor and reproducibility,and most importantly,to greater understanding and not simply knowing.

Effect of Chromium on Oxidative Damage and Antioxidant Capacity of Ctenopharyngodon idellus

[Objective] This study aimed to investigate the effect of chromium on ox- idative damage and antioxidant capacity of Ctenopharyngodon idellus （grass carp）. [Method] The grass carps were treated with hexavalent chromium （Cr^6＋） solution at concentrations of 0, 7.23, 14.47, 28.94 mg/L, and then the content of malondialde- hyde （MDA）, the level of total antioxidative capacity （T-AOC） and the activity of gtu- tathione-S-transferase （GST） in the hepatopancreas of grass carp were determined after 96 hours in different treatment groups. [Result] The content of MDA presented increasing trend with the increase of exposure Cr^6＋ concentrations. The activity of T-AOC increased firstly, then decreased with the increasing Cr^6＋ exposure concentra- tions, showing that the level of T-AOC was induced in tow and medium concentrat ions （7.23 and 14.47 mg/L）, but inhibited in high concentrations （28.94 mg/L）. Among the exposure groups, the level of T-AOC in medium concentration group （14.47 mg/L） was significantly higher than the control （P〈0.05）. Except the low concentration groups （7.23 mg/L） of which the GST activity was slightly induced, the GST activities of the other groups all showed downward trend with increasing Cr^6＋ levels, and the activity of GST in 28.94 mg/L group was significantly lower than the control group （P〈0.05）. [Conclusion] Cr^6＋ could cause large oxidative damage in the hepatopancreas of grass carp, thus poisoning it, and Cr^6＋ may further damage the organizational structure and physiological function of grass carp.

Increased oxidative stress and oxidative damage associated with chronic bacterial prostatitis

Aim： To investigate whether chronic bacterial prostatitis might increase oxidative stress and oxidative damage in chronic bacterial prostatitis patients （CBPP）, and to explore its possible mechanism. Methods： Enrolled in a casecontrol study were 70 randomly sampled CBPP and 70 randomly sampled healthy adult volunteers （HAV）, on whom plasma nitric oxide （NO）, vitamin C （VC）, vitamin E （VE） and β-carotene （β-CAR） level, erythrocyte malondialdehyde （MDA） level, as well as erythrocyte superoxide dismutase （SOD）, catalase （CAT） and glutathione peroxidase （GPX） activities were determined by spectrophotometry. Results： Compared with the HAV group, values of plasma NO and erythrocyte MDA in the CBPP group were significantly increased （P 〈 0.001）; those of plasma VC, VE and β-CAR as well as erythrocyte SOD, CAT and GPX activities in the CBPP group were significantly decreased （P 〈 0.001）. Findings from partial correlation for the 70 CBPP showed that with prolonged course of disease, values of NO and MDA were gradually increased （P 〈 0.001）, and those of VC, VE, β-CAR, SOD, CAT and GPX were gradually decreased （P 〈 0.05- 0.001）. The findings from stepwise regression for the 70 CBPP suggested that the model was Y= -13.2077 ＋ 0.1894MDA ＋ 0.0415NO - 0.1999GPX, F = 18.2047, P 〈 0.001, r = 0.6729, P 〈 0.001. Conclusion： The findings suggest that there exist increased oxidative stress and oxidative damage induced by chronic bacterial prostatitis in the patients, and such phenomenon was closely related to the course of disease.

Dietary resveratrol attenuation of intestinal inflammation and oxidative damage is linked to the alteration of gut microbiota and butyrate in piglets challenged with deoxynivalenol

Background:Deoxynivalenol(DON)is a widespread mycotoxin that induces intestinal inflammation and oxidative stress in humans and animals.Resveratrol(RES)effectively exerts anti-inflammatory and antioxidant effects.However,the protective effects of RES on alleviating DON toxicity in piglets and the underlying mechanism remain unclear.Therefore,this study aimed to investigate the effect of RES on growth performance,gut health and the gut microbiota in DON-challenged piglets.A total of 64 weaned piglets[Duroc×(Landrace×Yorkshire),21-d-old,6.97±0.10 kg body weight(BW)]were randomly allocated to 4 treatment groups(8 replicate pens per treatment,each pen containing 2 males;n=16 per treatment)for 28 d.The piglets were fed a control diet(CON)or the CON diet supplemented with 300 mg RES/kg diet(RES group),3.8 mg DON/kg diet(DON)or both(DON+RES)in a 2×2 factorial design.Results:DON-challenged piglets fed the RES-supplemented diet had significantly decreased D-lactate concentrations and tumor necrosis factor alpha(TNF-α)and interleukin 1 beta(IL-1β)mRNA and protein expression,and increased zonula occludens-1(ZO-1)mRNA and protein expression compared with those of DON-challenged piglets fed the unsupplemented diet(P<0.05).Compared with unsupplemented DON-challenged piglets,infected piglets fed a diet with RES showed significantly decreased malondialdehyde(MDA)levelsand increased mRNA expression of antioxidant enzymes and antioxidant genes(i.e.,GCLC,GCLM,HO-1,SOD1 and NQO-1)and glutamatecysteine-ligase modulatory subunit(GCLM)protein expression(P<0.05).Moreover,RES supplementation significantly abrogated the increase in the proportion of TUNEL-positive cells and the protein expression of caspase3 in DON-challenged piglets(P<0.05).Finally,RES supplementation significantly increased the abundance of Roseburia and butyrate concentrations,while decreasing the abundances of Bacteroides and unidentified-Enterobacteriaceae in DON-challenged piglets compared with DON-challenged piglets alone(P<0.05).Conclusions:RES supplementation improved gut health in DON-challenged piglets by strengthening intestinal barrier function,alleviating intestinal inflammation and oxidative damage,and positively modulating the gut microbiota.The protective effects of RES on gut health may be linked to increased Roseburia and butyrate concentrations,and decreased levels of Bacteroides and unidentified-Enterobacteriaceae.

3,4-Methylenedioxymethamphetamine(MDMA)Abuse Markedly Inhibits Acetylcholinesterase Activity and Induces Severe Oxidative Damage and Liperoxidative Damage

Objective To investigate whether 3,4-methylenedioxymethamphetamine (MDMA) abuse produces another neurotoxicity which may significantly inhibit the acetylcholinesterase activity and result in severe oxidative damage and liperoxidative damage to MDMA abusers. Methods 120 MDMA abusers (MA) and 120 healthy volunteers (HV) were enrolled in an independent sample control design, in which the levels of lipoperoxide (LPO) in plasma and erythrocytes as well as the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX) and acetylcholinesterase (AChE) in erythrocytes were determined by spectrophotometric methods. Results Compared with the average values of biochemical parameters in the HV group, those of LPO in plasma and erythrocytes in the MA group were significantly increased (P<0.0001), while those of SOD, CAT, GPX and AChE in erythrocytes in the MA group were significantly decreased (P<0.0001). The Pearson product-moment correlation analysis between the values of AChE and biochemical parameters in 120 MDMA abusers showed that significant linear negative correlation was present between the activity of AChE and the levels of LPO in plasma and erythrocytes (P<0.0005-0.0001), while significant linear positive correlation was observed between the activity of AchE and the activities of SOD, CAT and GPX (P<0.0001). The reliability analysis for the above biochemical parameters reflecting oxidative and lipoperoxidative damages in MDMA abusers suggested that the reliability coefficient (alpha) was 0.8124, and that the standardized item alpha was 0.9453. Conclusion The findings in the present study suggest that MDMA abuse can induce another neurotoxicity that significantly inhibits acetylcholinesterase activity and aggravates a series of free radical chain reactions and oxidative stress in the bodies of MDMA abusers, thereby resulting in severe neural, oxidative and lipoperoxidative damages in MDMA abusers.

Ozone Emitted During Copying Process-A Potential Cause of Pathological Oxidative Stress and Potential Oxidative Damage in the Bodies of Operators

To estimate the impact of copying on the indoor air quality, and to investigate whether ozone emitted during such a process induces pathological oxidative stress and potential oxidative damage in the bodies of operators. Methods 67 copying operators (CO) and 67 healthy volunteers (HV) were enrolled in a random control study, in which levels of lipoperoxide (LPO) in plasma and erythrocytes, and levels of vitamin C (VC), vitamin E (VE) and b-carotene (b-CAR) in plasma as well as activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) in erythrocytes were determined by spectrophotometric methods. Results Compared with the HV group, the average values of LPO in plasma and erythrocytes in the CO group were significantly increased (P<0.0001), while those of VC, VE and b-CAR in plasma as well as those of SOD, CAT and GPX in erythrocytes in the CO group were significantly decreased (P<0.0001). Pearson product-moment correlation analysis showed that with increase of ozone level in copying sites and duration of exposure to ozone, the values of LPO in plasma and erythrocytes in the bodies of operators were gradually increased,while those of VC, VE, b-CAR, SOD, CAT and GPX were decreased in the same manner. Odds ratio (OR) of risk of biochemical parameters reflecting potential oxidative damage of the copying operators ranged from 4.440 to 13.516, and 95 % CI of OR was from 2.113 to 34.061. Reliability coefficient () of the biochemical parameters used to reflect the potential oxidative damage of the operators was 0.8156, standardized item =0.9929, P<0.0001. Conclusion Findings in the present study suggest that there exist a series of free radical chain reactions and pathological oxidative stress induced by high dose ozone in the operators, thereby causing potential oxidative and lipoperoxidative damages in their bodies.

An Investigation of Oxidative DNA Damage in Pharmacy Technicians Exposed to Antineoplastic Drugs in Two Chinese Hospitals Using The Urinary 8-OHdG Assay

Objective To investigate oxidative DNA damage in pharmacy technicians preparing antineoplastic drugs at the PIVAS （Pharmacy Intravenous Admixture Service） in two Chinese hospitals. Methods Urinary 8-OHdG served as a biomarker. 5-Fluorouracil （5-FU） concentrations in air, masks and gloves were determined. The spill exposure of each PIVAS technician to antineoplastic drugs was investigated. Eighty subjects were divided into exposed group t, II, and control group I, II. Results 5-FU concentration ratios for gloves and masks in exposed group I were significantly higher than those in exposed group II （P〈0.05 or P〈0.01）. The average urinary 8-OHdG concentrations in exposed group I, control group I, exposed group II, and control group II were 24.69＋0.93, 20.68＋1.07, 20.57＋0.55, and 12.96_＋0.73 ng/mg Cr, respectively. Urinary 8-OHdG concentration in exposed group I was significantly higher than that in control group I or that in exposed group 11 （P〈0.02）. There was a significant correlation between urinary 8-OHdG concentrations and spill frequencies per technician （P〈0.01）. Conclusion There was detectable oxidative DNA damage in PIVAS technicians exposed to antineoplastic drugs. This oxidative DNA damage may be associated with their spill exposure experience and contamination of their personal protective equipment.

Effect of methylmercury on some neurotransmitters and oxidative damage of rats

In order to study the molecular mechanism of injury in rat organs induced by methylmercury, and the relationship between neurotransmitter and oxidative damage in the toxicity process of rat injury by methylmercury was studied. The control group was physiological saline of 0.9%, the concentration of exposure groups were 5 mg/(kg5d) and 10 mg/(kg5d) respectively. The content of AChE, ACh, NOS, NO, MDA, SOD, GSH-Px and GSH in different organs of rats were determined with conventional methods. The results showed that after exposure to methylmercury for 7 d, the mercury content in brain of exposure groups increased clearly and had significant difference compared with the control group(P<0.01). In rat's brain, serum, liver and kidney, the content of ACh and AChE were all decreased; the content of NOS and NO were all increased; the content of MDA was increased compared with the control group, the exposure groups had significant difference (P<0.01); the content of SOD, GSH and GSH-Px was decreased compared with the control group, the exposure groups had significant difference(P<0.01). It could be concluded that methylmercury did effect the change of neurotransmitter and free radical. They participated in the toxicity process of injury by methylmercury. The damage of neurotransmitter maybe cause the chaos of free radical and the chaos of free radical may also do more damage to neurotransmitter vice versa.

CYP2E1-dependent hepatotoxicity and oxidative damage after ethanol administration in human primary hepatocytes

AIM： To observe the relationship between ethanol-induced oxidative damage in human primary cultured hepatocytes and cytochrome P450 2E1 （CYP2E1） activity, in order to address if inhibition of CYP2E1 could attenuate ethanol- induced cellular damage. METHODS： The dose-dependent （25-100 mmol/L） and time-dependent （0-24 h） exposures of primary human cultured hepatocytes to ethanol were carried out. CYP2E1 activity and protein expression were detected by spectrophotometer and Western blot analysis respectively. Hepatotoxicity was investigated by determination of lactate dehydrogenase （LDH） and aspartate transaminase （AST） level in hepatocyte culture supernatants, as well as the intracellular formation of malondialdehyde （MDA）. RESULTS： A dose-and time-dependent response between ethanol exposure and CYP2E1 activity in human hepatocytes was demonstrated. Moreover, there was a time-dependent increase of CYP2E1 protein after 100 mmol/L ethanol exposure. Meanwhile, ethanol exposure of hepatocytes caused a time-dependent increase of cellular MDA level, LDH, and AST activities in supernatants. Furthermore, the inhibitor of CYP2E1, diallyl sulfide （DAS） could partly attenuate the increases of MDA, LDH, and AST in human hepatocytes. CONCLUSION： A positive relationship between ethanolinduced oxidative damage in human primary cultured hepatocytes and CYP2E1 activity was exhibited, and the inhibition of CYP2E1 could partly attenuate ethanol-induced oxidative damage.

Oxidative stress and damage induced by abnormal free radical reactions and IgA nephropathy

Objective: To estimate the oxidative stress and oxidative damage induced by abnormal free radical reactions in IgA nephropathy (IgAN) patients' bodies. Methods: Seventy-two IgA N patients (IgANP) and 72 healthy adult volunteers (HAV) were enrolled in a random control study design, in which the levels of nitric oxide (NO) in plasma, lipoperoxide (LPO) in plasma and in erythrocytes, and vitamin C (VC), vitamin E (VE) and β-carotene (β-CAR) in plasma as well as the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) in erythrocytes were determined with spectrophotometric mothods. Results: Compared with the HAV group, the averages of NO in plasma, and LPO in plasma and in erythrocytes in the IgANP group were significantly increased (P＜0.0001), while those ofVC, VE and β-CAR in plasma as well as those of SOD, CAT and GPX in erythrocytes in the IgANP group were significantly decreased (P＜0.0001). Linear correlation analysis showed that with the increase of the values of NO, and LPO in plasma and in erythrocytes, and with the decrease of those ofVC, VE, β-CAR,SOD, CAT and GPX in the IgAN patients, the degree of histological damage of tubulointerstitial regions was increased gradually (P＜0.0001); and that with the prolongation of the duration of disease the values of NO, and LPO in plasma and erythrocytes were increased gradually, while those of VC, VE, β-CAR, SOD, CAT and GPX were decreased gradually (P＜0.005). The discriminatory correct rates of the above biochemical parameters reflecting oxidative damage of the IgAN patients were 73.8%-92.5%, and the correct rates for the HAV were 70.0%-91.3% when independent discriminant analysis was used; and the correct rate for the IgAN patients was increased to 98.8%, the correct rate for the HAV was increased to 100% when stepwise discriminant analysis was used. The above biochemical parameters' reliability coefficient (alpha) were used to estimate the oxidative damage of the IgAN patients as 0.8145, the standardized item alpha=0.9730, F=53273.5681, P＜0.0001. Conclusions: A series of free radical chain reactions caused serious pathological aggravation in the IgANP' bodies, thus resulting in oxidative damage in their bodies. In treating IgANP, therefore, it is necessary that suitable dose antioxidants should be supplemented to them so as to alleviate the oxidative damage in their bodies.

Oxidative stress and lipid peroxidation products:effect of pinealectomy or exogenous melatonin injections on biomarkers of tissue damage during acute pancreatitis

BACKGROUND:Melatonin (N-acetyl-5-methoxytripta-mine) is a free radical scavenger and a strong antioxidant,secreted by the pineal gland.In this study,we evaluated the effects of decreasing and increasing serum melatonin levels on malonyldialdehyde (MDA),superoxide dismutase (SOD),and reduced glutathione (GSH) levels in pancreatic tissue from rats with experimental acute pancreatitis.METHODS:Experimental acute pancreatitis was induced in three groups of Wistar albino rats (10 animals per group) by pancreatic ductal ligation.The first group had only acute pancreatitis and served as the control.Surgical pinealectomy was added to acute pancreatitis in the second group,removing the source of endogenous melatonin (low melatonin levels group).The third group was given 0.1 ml daily intraperitoneal injections of 20 mg/ml melatonin solution for one week (high melatonin levels group).The effects of melatonin levels were evaluated by comparison of the levels of MDA,SOD,and GS in pancreatic tissue.RESULT:We found that intraperitoneal melatonin injections decreased the levels of MDA and increased the levels of SOD and GSH in pancreatic tissue.CONCLUSION:Exogenous melatonin has a preventive effect on lipid peroxidation and oxidative damage in acute pancreatitis.

Putrescine Plays a Positive Role in Salt-Tolerance Mechanisms by Reducing Oxidative Damage in Roots of Vegetable Soybean

Polyamines play important roles in plant tolerance to environmental stress. With the aim of investigating the possible involvement of putrescine （Put） in salt-tolerance mechanisms in vegetable soybean roots, exogenous Put （10 mmol L＂） and its biosynthetic inhibitor D-arginine （D-Arg） （0.5 mmol L-1） were added to nutrient solution when vegetable soybean （Glycine max L. cv. Huning 95-1） seedlings were exposed to 100 mmol L^-11 sodium chloride （NaCl）. The results showed that Put ameliorated but D-Arg aggravated the detrimental effects of NaCl on plant growth and biomass production. Under NaCl stress, levels of free, soluble conjugated and insoluble bound types of Put in roots of vegetable soybean were reduced, whereas those of free, soluble conjugated, and insoluble bound types of spermidine （Spd） and spermine （Spm） were increased. Exogenous Put eliminated the decrease in Put but promoted the increase of Spd and Spm. However, these changes could be reversed by D-Arg. Under NaCl stress, activities of arginine decarboxylase （ADC）, S-adenosylmethionine decarboxylase （SAMDC）, diamine oxidase （DAO）, and polyamine oxidase （PAO） were induced, with exogenous Put promoting and D-Arg reversing these changes. Furthermore, NaCl stress decreased activities of antioxidant enzymes. Exogenous Put alleviated but D-Arg exaggerated these effects of NaCl stress, resulting in the same changes in membrane damage and reactive oxygen species （ROS） production. These results indicated that Put plays a positive role in vegetable soybean roots by activating antioxidant enzymes and thereby attenuating oxidative damage.

Oxidative Damage to Lung Tissue and Peripheral Blood in Endotracheal PM_(2.5)-treated Rats

Objective To investigate the oxidative damage to lung tissue and peripherial blood in PM2.5-treated rats. Methods PM2.5 samples were collected using an auto-sampling instrument in summer and winter. Treated samples were endotracheally instilled into rats. Activity of reduced glutathione peroxidase （GSH-Px） and concentration of malondialdehyde （MDA） were used as oxidative damage biomarkers of lung tissue and peripheral blood detected with the biochemical method. DNA migration length （μm） and rate of tail were used as DNA damage biomarkers of lung tissue and peripheral blood detected with the biochemical method. Results The activity of GSH-Px and the concentration of MDA in lung tissue significantly decreased after exposure to PM2.5 for 7-14 days. In peripheral blood, the concentration of MDA decreased, but the activity of GSH-Px increased 7 and 14 days after experiments. The two indicators had a dose-effect relation and similar changing tendency in lung tissue and peripheral blood. The DNA migration length （μm） and rate of tail in lung tissue and peripheral blood significantly increased 7 and 14 days after exposure to PM2.5. The two indicators had a dose-effect relation and similar changing tendency in lung tissue and peripheral blood. Conclusion PM2.5 has a definite oxidative effect on lung tissue and peripheral blood. The activity of GSH-Px and the concentration of MDA are valuable biomarkers of oxidative lung tissue damage induced by PM2.5. The DNA migration length （μm） and rate of tail are simple and valuable biomarkers of PM2 5-induced DNA damage in lung tissues and peripheral blood. The degree of DNA damage in peripheral blood can predict the degree of DNA damage in lung tissue.

Oxidative damage of primary cultured hippocampal neurons Does androgen have an antagonistic effect?

BACKGROUND： Evidence illustrates that androgen has a neuroprotective role. However, whether androgen also has the protective effect on hippocampal neurons during free radical mediated injury remains unclear. OBJECTIVE： To investigate the neuroprotective effect of androgen on hippocampal neurons during free radical damage. DESIGN, TIME AND SETTING： A controlled in vitro experiment was performed at the Department of Human Anatomy, Cell Culture Lab, and Neuroendocrinology Lab, Basic Medical School, Hebei Medical University from February to June 2009. MATERIALS： Testosterone was provided by Tianjin Jinyao Amino Acid Company, China. METHODS： Primary cultured neurons from 24 Sprague Dawley rats were randomly assigned into four groups： control, H202, testosterone, and testosterone （pre-added） plus H2O2 groups. MAIN OUTCOME MEASURES： The positive cell ratio of microtubule associated protein-Ⅱ and neuron specific enolase was determined by immunocytochemistry. Neuronal morphology was observed by hematoxylin-eosin staining and Nissl staining. Cell vitality and viability were determined using an inverted phase contrast microscope. The content of nitric oxide synthase, malondialdehyde, and superoxide dismutase were measured with a spectrophotometer. RESULTS： As compared with the control group, cell vitality and viability, and superoxide dismutase level were significantly decreased in the H202 group （P 〈 0.05）, while nitric oxide synthase and malondialdehyde levels were significantly increased （P 〈 0.05）. Neuronal vitality and viability as well as superoxide dismutase level in the testosterone plus H2O2 group were significantly greater than in the H2O2 group （P 〈 0.05）, and nitric oxide synthase and malondialdehyde levels were significantly less than in the H2O2 group （P〈 0.05）. CONCLUSION： Androgen partially reversed H2O2-induced neuronal damage and protected neurons.